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51 Cards in this Set
- Front
- Back
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what drugs do you use for nuerostimulatory hyperexcitability states?
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phenothiazines
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what are the 4 mechanisms of cardiovascular toxicity?
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alt impulse formation of conduction
alt cell membrane direct damage to myocardial cells induced vascular changes |
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what do you monitor w/ cardiac monitoring?
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-regular auscultation
-ECG should be standard for suspected toxicoses with clinical sign in small - animal -pulse-ox with rate info -blood pressure monitoring |
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how would you treat symptomatic hypotension?
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fluid management
mild-mod crystalloids 40-90 mls/kg severe- colloids, hypertonic saline, blood products dobutamine dopamine /epinephrine |
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how would you treat symptomatic bradycardia? Rarely need to...
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atropine/ glyccopyrolate
for cases with potential clinical sequela isoproteranol dopamine |
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how do you treat symptomatic hypertension & tachycardia?
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fluids
B-blockersfor primary tachycardia if associated with neuroexcitatory drugs (environment quiet, admin benzos & anoxiolytics) |
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name the souce of toxin that causes ventricular arrythmias & tachycardia?
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digoxin, digitalis glycoside (foxglove) intoxication, lilly of the valley, azalea, yews & many more
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treatment for digoxin associated ventricular arrythmias?
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goal is to prevent vetnricular fibrillation (vent rate high 100s dogs low 200s cats, multiform complexes, loss of T wave)
correct underlying electrolyte disturbances (hypokalemia, hypomagnesemia) use lidocaine or procainamide digibind |
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what are the hematotoxicoses?
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hemoglobin toxins (methemoglobinemia), erythrocyte toxins (hemolytics)
coagulation toxins |
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what are the methemoglobinemia inducing toxins?
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acetaminophen
nitrites chlorates resorcinol naphthalene other NSAIDs |
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what is the triad of oxidative damage to RBCs?
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hemoglobins destruction (methemoglobinemia)
heinz body formation hemolysis |
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who is resistant to methemoglobinemia?
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rodents/lab animals
high activity of enzyme methemoglobin reductase |
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what are the clinical signs of methemoglobin toxicosis?
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blood is dark brown (eventually mm too), cyanosis and dyspnea (30-40% mild anoxic signs)
weakness and recumbancy |
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how are heinz bodies formed?
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denatured hemoglobin covalently bound to erythrocyte membrane
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what do heinz bodies do to erythrocytes?
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reduce flexability and deformability, increase phagocytosis in RES, removal from circ and hemolysis will be clinically noted when excessive
sequela of renal damage |
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what is the triad of oxidative damage to RBCs?
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hemoglobins destruction (methemoglobinemia)
heinz body formation hemolysis |
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who is resistant to methemoglobinemia?
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rodents/lab animals
high activity of enzyme methemoglobin reductase |
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what are the clinical signs of methemoglobin toxicosis?
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blood is dark brown (eventually mm too), cyanosis and dyspnea (30-40% mild anoxic signs)
weakness and recumbancy |
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how are heinz bodies formed?
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denatured hemoglobin covalently bound to erythrocyte membrane
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what do heinz bodies do to erythrocytes?
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reduce flexability and deformability, increase phagocytosis in RES, removal from circ and hemolysis will be clinically noted when excessive
sequela of renal damage |
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oxidative toxins treatment?
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supportive: ox therapy
fluids- dilute hemoglobinuria consider blood transfusions (after antidote admin) oxyglobin admin in dogs (bovine hemoglobin) reducing agents: ascorbic acid, sodium sulfate N-acetylcystine (acetominophen esp), source of sulfhydryl groups on hemoglobin and glutathione replacement |
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N-acetyl-parabenzoquinoneimine is also known as what? what is this metabolite associated with?
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NAPQI and acetominophen tox
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what is the MOT of acetominophen?
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oxidation of RBCs and hemoglobin
liver-build up of metabolite in liver leads to hepatic necrosis (binds covalently to cellular macromolecules) |
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what are the clinical signs of acetominophen tox in cats?
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cyanosis within 4-12hours (methemoglobinemia and anemia) follows the oxidative triad
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what does acetominophen tox cause in hepatic necrosis?
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hepatic necrosis
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what is the MOT of acetominophen?
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oxidation of RBCs and hemoglobin
liver-build up of metabolite in liver leads to hepatic necrosis (binds covalently to cellular macromolecules) |
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what are the clinical signs of acetominophen tox in cats?
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cyanosis within 4-12hours (methemoglobinemia and anemia) follows the oxidative triad
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what does acetominophen tox cause in hepatic necrosis?
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hepatic necrosis
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how do you treat acetominophen with?
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decontamination w/i 4 hrs (emesis, gastric lavage, activated charcoal, cathartics)
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what is the antidote for acetominophen?
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acetlcysteine never too late in cats
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what is the supplimentary anitidote for acetominophen?
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s-adenosylmethionine (SAMe) provides a source of sulfur donation
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what is possible with acetominophen in dogs that is not in cats?
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KCS at low doses focus on the liver toxicity is the focus
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***name the hemolytic toxins?
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onion/garlic, acer rubrum (red maple), etc..
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what are hemolytic toxin clinical signs?
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depression, anemia, icterus, hemoglobinemia, hemoglobinuria, muddy mm
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how do you diagnose hemolytic toxins exposure?
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PCV:TP methemoglobinemia, heinz bodies
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Acer rubrum tox tx?
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recent: gastric lavage cathartics
supportive care: diuresis, transfusion, oxygen therapy antioxidant therapy?? ascorbic acid |
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what products causeNSAID toxicosis ?
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asprin, non specific cox inhibitors, ibuprofen, naproxen, ketoprofen, carprofen, phenylbutazone
cox2 specific- meloxicam, deracoxib, celecoxib |
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what is MOT of NSAIDs?
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acute drop in protective pg activity
oxidation of hemoglobin (cats) red circ to critical areas gastric mucosa, renal medulla incr tubular sodium and water resorption |
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what is initial tx for NSAID tox?
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emetics (poss cathartics, repeat doses)
venous line |
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with NSAID tox what is the system assessment & Tx?
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GI- vomiting (antiemetic, metaclopramide)
ulceration- PCV:TP & CBC, look for blood loss (transfuse, oxyglobin) begin gastroprotecants (sucralfate, omeprazole +/- famotide, misoprostol) renal condition- ensure hydration is ok (fluids 2-3X maintenance), poor hydration leads to papillary necrosis, poor circ, observe for PU/PD, USG for baseline at least, assess for azotemia & hyperkalemia hemotologic- may be anemic (prolonged bleeding times, possible active bleeding) hepatopathies- usually in cases of chronic exposure |
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what is aleves slogan
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all day long all day strong--- long T1/2
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what are teh predisposing factors to NSAID effects?
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decr renal function, GI dz, age, stress, hypotension, cardiac dz, dehydration
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what are the 2 kinds of hepatic toxicities?
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intrinsic & idiosyncratic (both are cytotoxic)
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what are the 2 kinds of intrinsic hepatoxicities?
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direct and indirrect
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what diagnostics are used in acute hepatic toxicities?
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CBC, serum biochem (ALT, AP, GGT, SDH, inc bile acids, hypoglycemia), urinalysis (urobilinogen is high), coagulopathy
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what is tx for hepatic toxicities?
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hepatic encephalopathy- release of N compounds, maintain high carb (low protein diet), lactulose (traps NH3 as NH4 in gut and decreases prod by gut), CNS as above
coagulopathy- loss of clotting factors (vit K, transfusions of plasma or plasma products, oxyglobin) fluids- maintian glucose hepatoprotectants (N-acetylcysteine, glutathione source of antiox, SAMe, vit Eas antiox) |
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what should you consider when txing a hepatic toxicity?
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refrain from using drugs that require extensive hepatic metabolism
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where do you find xylitol?
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sugar free candies and gum
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what are clinical signs of xylitol?
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profound hypoglycemia, lethargy, seizures, hypokalemia
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how do you tx for xylitol?
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decontaminate (emesis, active charcoal),
blood glucose + liver chem (tx hypoglycemia stat, fluids w/ dextrose, oral corn-syrup & on gums), SAMe for liver function, continue monitoring hepatic function( therapies), continual monitoring for 12-24 hrs post contamination |
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who shoudl you consult with toxicities?
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animal poison control center (aspca)
pet poison help line |
